Proper cardiac function relies on the synchronized contraction of the heart at regular intervals. When normal cardiac rhythm is initiated at the sinoatrial node, the heart is said to be in sinus rhythm. However, when the heart experiences irregularities in its coordinated contraction, due to electrophysiologic disturbances caused by a disease process or from an electrical disturbance, the heart is denoted to be arrhythmic. The resulting cardiac arrhythmia impairs cardiac efficiency and can be life-threatening.
Cardiac arrhythmias originating in the atria of the heart are called supra-ventricular tachyarrhythmias (SVTs). SVTs take many forms, including atrial fibrillation and atrial flutter. Both conditions are characterized by rapid, uncoordinated contractions of the atria. Besides being hemodynamically inefficient, the rapid contractions of the atria can also adversely affect the ventricular rate. This occurs when the aberrant impulse in the atria are transmitted to the ventricles. It is then possible for the aberrant atrial signals to cause irregular ventricular activation and even induce ventricular tachyarrhythmias.
Cardiac arrhythmias occurring in the ventricular region of the heart, by way of further example, are called ventricular tachyarrhythmias. Ventricular tachycardia (VTs), for example, are conditions denoted by a rapid heart beat, 150 to 250 beats per minute, that has its origin in some abnormal location with the ventricular myocardium. The abnormal location typically results from damage to the ventricular myocardium from a myocardial infarction. Ventricular tachycardia can quickly degenerate into ventricular fibrillation (VF). Ventricular fibrillation is a condition denoted by extremely rapid, non synchronous contractions of the ventricles. This condition is fatal unless the heart is returned to sinus rhythm within a few minutes.
Pro-arrhythmia has been defined as the provocation of a new arrhythmia or the aggravation of a pre-existing arrhythmia during therapy with a drug at doses or plasma concentrations below those considered toxic. Suggested criteria for pro-arrhythmia include: the new appearance of a sustained ventricular tachyarrhythmia; change from a nonsustained to a sustained ventricular tachyarrhythmia; acceleration of tachycardia rate; or the new appearance of a clinically significant bradyarrhythmia or conduction defect. Pro-arrhythmia can be the direct result of a drug's electrophysiologic effects on conduction velocity, refractoriness, and automaticity. However, it may also be the result of metabolic abnormalities, changes in autonomic state, or drug/drug interactions that amplify or alter the drug's electrophysiologic effects.
SVT Atrial Fibrillation (AF) is the most common arrhythmia in man. AF may be terminated by defibrillation shocks or by anti-arrhythmic drugs. Defibrillation shocks are successful at terminating AF in the majority of patients, however, they have physical/psychological side effects of pain or discomfort, low patient tolerance, and the potential for ventricular pro-arrhythmia. Anti-arrhythmic drugs can also be highly successful at terminating AF. However, drugs present a significant risk of ventricular pro-arrhythmia in the hours-days following chemical cardioversion. The ventricular pro-arrhythmia observed following attempted (successful or unsuccessful) chemical cardioversion of AF is typically polymorphic ventricular tachycardia (e.g., Torsade-de-Pointes). Torsade is known to be exacerbated by ventricular pauses and bradycardia. Importantly, Torsade-de-Pointes can be prevented by pacing modes that eliminate ventricular pauses and bradycardia.
AF patients who are candidates for cardioversion have frequent or recurring episodes of AF and therefore will require future electrical or chemical cardioversion to maintain normal sinus rhythm. Chemical cardioversion may allow for the alleviation of AF burden with elimination of the single largest drawback of defibrillation therapy—patient pain perception. However, the pro-arrhythmia risk associated with chemical cardioversion is significant (˜5%). As a result, following chemical cardioversion, patients may remain in the hospital for some number of hours or days to be monitored for the presence of ventricular arrhythmias.
There exists a need for improved systems and methods for treating cardiac arrhythmias and other adverse cardiac conditions, including adverse non-arrhythmic conditions. There exists a further need for such systems and methods that address the increased risk of pro-arrhythmia following delivery of chemical cardioversion. The present invention fulfills these and other needs.